Genazzani A A, Empson R M, Galione A
Department of Pharmacology, University of Oxford, United Kingdom.
J Biol Chem. 1996 May 17;271(20):11599-602. doi: 10.1074/jbc.271.20.11599.
Ca2+ mobilization from intracellular stores constitutes an important mechanism for generating cytoplasmic Ca2+ signals. Inositol trisphosphate (InsP3) and ryanodine receptors are the two families of intracellular Ca2+ release channels that have been identified, which may be regulated by separate intracellular messengers, InsP3, and cyclic adenosine 5'-diphosphate ribose, respectively. A third molecule, nicotinic acid adenine dinucleotide phosphate (NAADP), has recently been recognized as a potent Ca2+ releasing agent in sea urchin eggs and microsomes. We now report that non-releasing concentrations of NAADP fully and irreversibly inactivate the NAADP-sensitive Ca2+ release mechanism. This phenomenon occurred both in intact sea urchin eggs and in homogenates and is not shared by either InsP3 or cyclic adenosine 5'-diphosphate ribose. The novel properties of this Ca2+ release mechanism, giving a one-shot Ca2+ release, may be suited to irreversible cellular events.
从细胞内储存库动员Ca2+是产生细胞质Ca2+信号的重要机制。肌醇三磷酸（InsP3）和兰尼碱受体是已被鉴定的两类细胞内Ca2+释放通道，它们可能分别受细胞内信使InsP3和环腺苷5'-二磷酸核糖的调节。第三种分子，烟酰胺腺嘌呤二核苷酸磷酸（NAADP），最近被认为是海胆卵和微粒体中一种有效的Ca2+释放剂。我们现在报告，非释放浓度的NAADP能完全且不可逆地使NAADP敏感的Ca2+释放机制失活。这种现象在完整的海胆卵和匀浆中均会发生，且InsP3或环腺苷5'-二磷酸核糖都不会出现这种情况。这种Ca2+释放机制的新特性，即一次性Ca2+释放，可能适用于不可逆的细胞事件。
